FROM THE ARCHIVES – Kayexalate: What is it and does it work?

November 7, 2013

Please enjoy this post from the archives dated December 1, 2010

By Todd Cutler, MD

Faculty Peer Reviewed

A 62-year-old male is hospitalized with an acute congestive heart failure exacerbation. On hospital day three, the patient’s symptoms have significantly improved with twice daily furosemide 80mg IV. He is continued on IV diuretics and aggressive electrolyte repletion. On day five of his admission, his basic metabolic panel is significant for a creatinine of 2.3 mg/dL (increased from 1.3 on admission) and a potassium concentration of 5.9 mEq/L. His EKG is unchanged from admission. His furosemide is discontinued and he is given 15g of Kayexalate. Overnight he has a large bowel movement. The next morning his creatinine is 1.9 mg/dL and his potassium is 5.1 mEq/L.

In 1961, an uncontrolled study evaluated 32 patients with renal failure. Patients received either oral or rectally administered SPS while their intake of dietary potassium was tightly controlled. Patients were treated and monitored for varying lengths of time with one patient receiving SPS three times weekly for 280 days. Over the first 24 hours, plasma potassium concentrations decreased 1.0 mEq/L and 0.8 mEq/L in patients receiving oral and rectal SPS, respectively, with a few patients developing hypokalemia. The authors also reported complete reversion of abnormal EKG findings after SPS administration.[6]

An accompanying report in the same journal evaluated ten patients with renal failure who were treated for five days with either an SPS and sorbitol mixture or sorbitol alone. Prior to this study, it had been noted that an adverse effect of SPS was the induction of constipation leading to, in some cases, fecal impaction. A proposed solution to this problem involved the co-administration of sorbitol, an osmotic laxative, at a concentration of 70%, speeding delivery of SPS to the colon where the majority of ion-exchange activity was believed to occur while simultaneously inducing defecation – ultimately, the desired diuretic effect of the drug.

In the study, both patients who received the co-administered formulation and sorbitol alone, demonstrated decreased serum potassium concentrations. Furthermore, sodium concentrations were increased in patients who received SPS with sorbitol but not with the sorbitol control. The authors noted, “That this rise is caused by the sodium released from the resin in exchange for potassium is evident since there is no elevation of serum sodium when sorbitol is used alone,” while ultimately concluding that, “sorbitol alone is as effective as a combination of resin and sorbitol in removing potassium, or more so. However, sorbitol alone necessitated a greater volume of debilitating diarrhea. In either case the predictability of the fall in serum potassium was impressive.”[7]

Since the 1960s, investigations into the efficacy of SPS in treating hyperkalemia have been limited. One small study in 1998 showed no changed in serum potassium concentration after a single dose of SPS or a placebo both with and without a sorbitol additive.[8] The efficacy of SPS and any additive effect of sorbitol on serum potassium concentrations have never been elucidated in larger studies. Meanwhile, SPS became widely accepted as a means for treating hyperkalemia based on the results of uncontrolled reports and empiric observations.

The dearth of clinical evidence supporting the efficacy of SPS prompted the authors of a recent commentary in the Journal of the American Society of Nephrology to call for careful consideration before using SPS remarking, “It would be wise to exhaust other alternatives for managing hyperkalemia before turning to these largely unproven and potentially harmful therapies.”xiii The utilization of dietary restriction, diuretics, bicarbonate, beta-agonists, insulin and dextrose along with a careful investigation into the etiology of an individual patient’s hyperkalemia may obviate the perceived need for SPS administration. Until future studies clarify a role for this controversial drug, physicians should take into account the compiled evidence when weighing of the risks and benefits of SPS administration.

Special thanks to Dr. John Papadopoulus for his helpful commentary and assistance in the drafting of this article.

Kayexalate: What is it and does it work?

Commentary by Dr. John Papadopoulos

The skill to select and dose an optimal pharmacotherapeutic regimen to treat our patients develops over the course of one’s professional career and during our training. When learning about a medication, we focus on pharmacology, pharmacokinetics, potential adverse events, and data to support use in clinical practice. Unfortunately, we have a paucity of data for guidance when using medications developed and marketed before the rigor of our current drug review standards. The use of kayexalate in the management of hyperkalemia has been propagated by bedside teaching and without the rigor of evidence-based clinical trials. Dr. Cutler cogently summarizes the available literature and highlights the potential complications of kayexalate.

In my experience, kayexelate (per os and per rectum) is able to lower potassium levels modestly over the course of a few hours. It is a second-line agent that may be used when there is a need to lower total body potassium, as other interventions (except renal replacement therapies) temporarily move potassium into intracellular fluid.

Dr. Cutler is a second year resident at NYU Langone Medical Center and co-editor, pharmacology section of Clinical Correlations

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